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Epithelium is one of the four basic tissue types (the other three are muscle tissue, nerve tissue, and connective tissue). It is found throughout the body—covering it; lining organs, vessels, and cavities; and forming glands. It absorbs nutrients, transports electrolytes, secretes hormones, and regulates body temperature by producing sweat. We begin with some general principles of how epithelial tissue is organized, and then we describe its various components. After listening to this AudioBrick, you should be able to: List the two types of epithelium (covering/lining and glandular) and describe their functions. Describe the structure and histologic features of epithelial tissue. Explain how covering/lining epithelium is classified. Describe the histologic features of glandular epithelium. Describe the five types of epithelial intercellular junctions. You can also check out the original brick on the Histology of Epithelial Tissue from our Musculoskeletal, Skin, and Connective Tissue collection, which is available for free. Learn more about Rx Bricks by signing up for a free USMLE-Rx account: www.usmle-rx.com You will get 5 days of full access to our Rx360+ program, including nearly 800 Rx Bricks. After the 5-day period, you will still be able to access over 150 free bricks, including the entire collections for General Microbiology and Cellular and Molecular Biology. *** If you enjoyed this episode, we'd love for you to leave a review on Apple Podcasts. It helps with our visibility, and the more med students (or future med students) listen to the podcast, the more we can provide to the future physicians of the world. Follow USMLE-Rx at: Facebook: www.facebook.com/usmlerx Blog: www.firstaidteam.com Twitter: https://twitter.com/firstaidteam Instagram: https://www.instagram.com/firstaidteam/ YouTube: www.youtube.com/USMLERX Learn how you can access over 150 of our bricks for FREE: https://usmlerx.wpengine.com/free-bricks/
In this episode, we explore the crucial role of the protective mucus layer in maintaining intestinal lining integrity, highlighting how it shields the epithelial cells from harmful substances and supports overall digestive function. We dive into the components and functions of mucins, goblet cells, and secretory IgA, explaining their contributions to gut immunity and barrier integrity. Additionally, we discuss strategies for supporting mucus production centered around butyrate, N-acetyl glucosamine, and plant-derived mucilage. Topics: 1. Introduction: Overview of the Gastrointestinal Mucus Layer - Importance of the mucus secretions in forming a protective layer - Brief review of the gastrointestinal lining and its structure 2. The Mucosal Layer and Its Components - The mucus layer on the epithelial cells of the mucosa - Four main layers of the intestinal wall, focusing on the mucosa - Epithelium: absorptive enterocytes and mucus-secreting goblet cells - Lamina propria: connective tissue rich in immune cells, blood vessels, and lymphatics - Smooth muscle aiding in subtle movements - Submucosa: thicker connective tissue layer with blood vessels, nerves, and lymphatics 3. Dual Function of the Mucus Layer - Physical barrier preventing pathogens and toxins from reaching epithelial cells - Biochemical barrier housing antimicrobial peptides and immunoglobulins 4. Goblet Cells and Their Role in Mucin Production - Goblet cells: specialized epithelial cells producing mucins - Distribution of goblet cells from small to large intestine - Importance of goblet cells in maintaining the mucus barrier 5. Mucins: Structure and Glycosylation - Glycosylation and its role in mucus properties and host-microbiota interactions - Commensal bacteria and their interactions with mucins (e.g., Bacteroides and Akkermansia muciniphila) 6. The Importance of Controlled Mucin Degradation - Mutualistic relationship between mucin-degrading bacteria and the host - Risks of dysregulated mucin degradation, leading to dysbiosis and leaky gut 7. Secretory IgA and Its Role in Gut Immunity - Overview of secretory IgA (sIgA) and its production - sIgA's mechanism of neutralizing pathogens "without inflammation" - Immune exclusion as a defense mechanism to maintain gut barrier integrity 8. Recap: The Dynamic Nature of the Mucus Layer - Continuous renewal of the mucus layer and the role of goblet cells and plasma cells - Importance of regular mucus turnover for maintaining a healthy gut barrier 9. Supporting Gastrointestinal Mucus Production - Short-chain fatty acids (SCFAs) and their role in stimulating mucus production - Butyrate and its effects on goblet cells and epithelial repair - N-Acetyl Glucosamine (NAG) as a supplement to support mucin glycosylation 10. Supporting the Intestinal Lining After Dysbiosis or Increased Permeability - Mucilage and its role in coating and soothing mucosal surfaces - Plant-derived mucilage from slippery elm and marshmallow root - Physical protection provided by mucilage - Soothing effects on inflamed tissues and promoting smooth digestion Thank you to our episode sponsor: 1. Check out Daily Nouri and use code CHLOE20 for 20% off your order. Thanks for tuning in! Get Chloe's Book Today! "75 Gut-Healing Strategies & Biohacks" Follow Chloe on Instagram @synthesisofwellness Follow Chloe on TikTok @chloe_c_porter Visit synthesisofwellness.com to purchase products, subscribe to our mailing list, and more! --- Support this podcast: https://podcasters.spotify.com/pod/show/chloe-porter6/support
Dr. Peter Moore chats with Dr. Marilia Zuttion on her article, "Interstitial Macrophages Mediate Efferocytosis of Alveolar Epithelium during Influenza Infection."
BUFFALO, NY- July 9, 2024 – A new #editorial paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 12, entitled, “Aging retinal pigmented epithelium: omics-based insights into vision decline.” In this new editorial, researchers Ioan V. Matei and Luminita Paraoan from Edge Hill University discuss vision decline with aging. Of all senses affected by aging, vision decline arguably has the most impactful relationship with overall wellbeing, health and personal autonomy. However, while the ensuing importance of vision loss has long been recognised from a public health perspective given an increasingly aging population, understanding the molecular and cellular mechanisms driving age-related pathological changes is still in its infancy. “This matter is, therefore, critical for tackling sensory impairment and ensuring healthy aging.” The retinal pigmented epithelium (RPE), the cellular monolayer located between the neuroretina and the highly vascularized choroid, from which it is separated by Bruch's membrane (BrM), has a critical role in human vision and performs essential functions throughout life for maintaining the retinal homeostasis. RPE is a specialised, fully differentiated tissue that is mitotically inactive, with no regenerative potential. Unsurprisingly, given all its characteristics, functions and metabolic demands, the RPE is particularly susceptible to aging, sustaining significant morphologic and physiologic changes. “Aging is recognised as the highest risk factor for age-related macular degeneration (AMD), the leading cause of adult visual impairment and blindness in the Northern Hemisphere, which is directly linked to specific pathological changes of the RPE located in the macula, i.e., the central part of retina; these changes, therefore, affect central vision required for reading, driving, and discerning details of pictures, faces, shapes and colors.” DOI - https://doi.org/10.18632/aging.205914 Corresponding author - Luminita Paraoan - Luminita.Paraoan@edgehill.ac.uk Video short - https://www.youtube.com/watch?v=_-zhhFjlQ4Y Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205914 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, RPE, vision, omics About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
There are only four tissues that make up the body (epithelial, connective, muscle and nervous). We should talk about epithelia and carcinoma.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.25.550535v1?rss=1 Authors: Sheridan, J., Grata, A., Suva, E. E., Bresteau, E., Mitchell, L. R., Mitchell, B. Abstract: The skin of Xenopus embryos contains numerous multiciliated cells (MCCs), which collectively generate a directed fluid flow across the epithelial surface essential for distributing the overlaying mucous. MCCs develop into highly specialized cells to generate this flow, containing approximately 150 evenly spaced centrioles that give rise to motile cilia. MCC-driven fluid flow can be impaired when ciliary dysfunction occurs, resulting in primary ciliary dyskinesia (PCD) in humans. Mutations in a large number of genes (~50) have been found to be causative to PCD. Recently, studies have linked low levels of Adenylate Kinase 7 (AK7) gene expression to patients with PCD; however, the mechanism for this link remains unclear. Additionally, AK7 mutations have been linked to multiple PCD patients. Adenylate kinases modulate ATP production and consumption, with AK7 explicitly associated with motile cilia. Here we reproduce an AK7 PCD-like phenotype in Xenopus and describe the cellular consequences that occur with manipulation of AK7 levels. We show that AK7 localizes throughout the cilia in a DPY30 domain-dependent manner, suggesting a ciliary function. Additionally, we find that AK7 overexpression increases centriole number, suggesting a role in regulating centriole biogenesis. We find that in AK7-depleted embryos, cilia number, length, and beat frequency are all reduced, which in turn, significantly decreases the tissue-wide mucociliary flow. Additionally, we find a decrease in centriole number and an increase in sub-apical centrioles, implying that AK7 influences both centriole biogenesis and docking, which we propose underlie its defect in ciliogenesis. We propose that AK7 plays a role in PCD by impacting centriole biogenesis and apical docking, ultimately leading to ciliogenesis defects that impair mucociliary clearance. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.23.550233v1?rss=1 Authors: Ikawa, K., Hiro, S., Kondo, S., Ohsawa, S., Sugimura, K. Abstract: Directional cell rearrangement is a critical process underlying correct tissue deformation during morphogenesis. Although the involvement of F-actin regulation in cell rearrangement has been established, the role and regulation of actin binding proteins (ABPs) in this process are not well understood. In this study, we investigated the function of Coronin-1, a WD-repeat actin-binding protein, in controlling directional cell rearrangement in the Drosophila pupal wing. Transgenic flies expressing Coronin-1-EGFP were generated using CRISPR-Cas9. We observed that Coronin-1 localizes at the reconnecting junction during cell rearrangement, which is dependent on actin interacting protein 1 (AIP1), an actin disassembler and a known regulator of wing cell rearrangement. Loss of Coronin-1 function reduces cell rearrangement directionality and hexagonal cell fraction. These results suggest that Coronin-1 promotes directional cell rearrangement via its interaction with AIP1, highlighting the role of ABPs in the complex process of morphogenesis. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.12.548725v1?rss=1 Authors: Song, A., Phandthong, R., Talbot, P. Abstract: Both spill over and spill back of SARS-CoV-2 virus have been reported on mink farms in Europe and the United States. Zoonosis is a public health concern as dangerous mutated forms of the virus could be introduced into the human population through spillback. The purpose of our study was to determine the SARS-CoV-2 entry mechanism using mink lung epithelial cell line (Mv1Lu) and to block entry with drug inhibitors. Mv1Lu cells were susceptible to SARS-CoV-2 viral pseudoparticle infection, validating them as a suitable disease model for COVID-19. Inhibitors of TMPRSS2 and of endocytosis, two pathways of viral entry, were tested to identify those that blocked infection. Dyngo4a, a small molecule endocytosis inhibitor, significantly reduced infection, while TMPRSS2 inhibitors had minimal impact, supporting the conclusion that the entry of the SARS-CoV-2 virus into Mv1Lu cells occurs primarily through endocytosis. The small molecule inhibitors that were effective in this study could potentially be used therapeutically to prevent SARS-CoV-2 infection in mink populations. This study will facilitate the development of therapeutics to prevent zoonotic transmission of SARS-CoV-2 variants to other animals, including humans. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
CHEST May 2023, Volume 163, Issue 5 Wiei-jie Guan, MD, and De Yun Wang, MD, join CHEST Podcast Moderator, Gretchen Winter, MD, to discuss the characteristics of motile ciliary disorder of the nasal epithelium and its association with disease severity and inflammatory endotypes in adults with bronchiectasis. DOI: https://doi.org/10.1016/j.chest.2022.11.022 Disclaimer: The purpose of this activity is to expand the reach of CHEST content through awareness, critique, and discussion. All articles have undergone peer review for methodologic rigor and audience relevance. Any views asserted are those of the speakers and are not endorsed by CHEST. Listeners should be aware that speakers' opinions may vary and are advised to read the full corresponding journal article(s) for complete context. This content should not be used as a basis for medical advice or treatment, nor should it substitute the judgment used by clinicians in the practice of evidence-based medicine.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.26.538408v1?rss=1 Authors: Bhat, S. A., Malla, A. B., Oddi, V., Sen, J., Bhandari, R. Abstract: Inositol hexakisphosphate kinases (IP6Ks) are enzymes that catalyse the synthesis of the inositol pyrophosphate 5-IP7 which is involved in the regulation of many physiological processes in mammals. The IP6K paralog IP6K1 is expressed at high levels in the mammalian testis, and its deletion leads to sterility in male mice. Here, we show that the loss of IP6K1 in mice causes a delay in the first wave of spermatogenesis. Testes from juvenile Ip6k1 knockout mice show downregulation of transcripts that are involved in cell adhesion and formation of the testis-specific inter-Sertoli cell impermeable junction complex known as the blood-testis barrier (BTB). We demonstrate that loss of IP6K1 in the mouse testis causes BTB disruption associated with transcriptional misregulation of the tight junction protein claudin 3, and subcellular mislocalization of the gap junction protein connexin 43. In addition to BTB disruption, we also observe loss of germ cell adhesion in the seminiferous epithelium of Ip6k1 knockout mice, ultimately resulting in premature sloughing of round spermatids into the epididymis. Mechanistically, we show that loss of IP6K1 in the testis enhances cofilin activity due to increased AKT/ERK and integrin signalling, resulting in destabilization of the actin-based cytoskeleton in Sertoli cells and germ cell loss. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Tim Fenton, Ph.D., University of Southampton, shares his work on the roles of APOBEC3 genes. Hear how he is investigating APOBEC regulation and function in keratinocytes. Series: "Stem Cell Channel" [Health and Medicine] [Show ID: 38724]
Tim Fenton, Ph.D., University of Southampton, shares his work on the roles of APOBEC3 genes. Hear how he is investigating APOBEC regulation and function in keratinocytes. Series: "Stem Cell Channel" [Health and Medicine] [Show ID: 38724]
Tim Fenton, Ph.D., University of Southampton, shares his work on the roles of APOBEC3 genes. Hear how he is investigating APOBEC regulation and function in keratinocytes. Series: "Stem Cell Channel" [Health and Medicine] [Show ID: 38724]
Tim Fenton, Ph.D., University of Southampton, shares his work on the roles of APOBEC3 genes. Hear how he is investigating APOBEC regulation and function in keratinocytes. Series: "Stem Cell Channel" [Health and Medicine] [Show ID: 38724]
Tim Fenton, Ph.D., University of Southampton, shares his work on the roles of APOBEC3 genes. Hear how he is investigating APOBEC regulation and function in keratinocytes. Series: "Stem Cell Channel" [Health and Medicine] [Show ID: 38724]
Tim Fenton, Ph.D., University of Southampton, shares his work on the roles of APOBEC3 genes. Hear how he is investigating APOBEC regulation and function in keratinocytes. Series: "Stem Cell Channel" [Health and Medicine] [Show ID: 38724]
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.27.534398v1?rss=1 Authors: Hernandez-Clavijo, A., Sanchez-Trivino, C. A., Guarneri, G., Ricci, C., Mantilla-Esparza, F. A., Gonzalez-Velandia, K. Y., Boscolo-Rizzo, P., Toffanelli, M., Bonini, P., Dibattista, M., Tirelli, G., Menini, A. Abstract: The COVID-19 pandemic brought attention to our limited understanding of human olfactory physiology. While the cellular composition of the human olfactory epithelium is similar to that of other vertebrates, its functional properties are largely unknown. We prepared acute slices of human olfactory epithelium from nasal biopsies and used the whole-cell patch-clamp technique to record electrical properties of cells. We measured voltage-gated currents in human olfactory sensory neurons and supporting cells, and action potentials in neurons. Additionally, inward currents and action potentials responses of neurons to a phosphodiesterase inhibitor indicated that the transduction cascade involves cAMP as a second messenger. Furthermore, responses to odorant mixtures demonstrated that the transduction cascade was intact in this preparation. This study provides the first electrophysiological characterization of olfactory sensory neurons in acute slices of the human olfactory epithelium, paving the way for future research to expand our knowledge of human olfactory physiology. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Tim Fenton, Ph.D., University of Southampton, shares his work on the roles of APOBEC3 genes. Hear how he is investigating APOBEC regulation and function in keratinocytes. Series: "Stem Cell Channel" [Health and Medicine] [Show ID: 38724]
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.02.530846v1?rss=1 Authors: Li, Y., Liu, C., Bai, X., Li, M., Duan, C. Abstract: The cell proliferation-quiescence decision plays fundamental roles in tissue formation and regeneration, and its dysregulation can lead to human diseases. In this study, we performed transcriptomics and genetic analyses using a zebrafish model to identify pathways and genes involved in epithelial cell quiescence-proliferation regulation. In this in vivo model, a population of GFP-labeled epithelial cells known as ionocytes were induced to reenter the cell cycle by a physiological stress. Transcriptomics analysis identified 1168 genes up-regulated and 996 genes down-regulated in the reactivated cells. GO and KEGG pathway analyses revealed that genes involved in transcription regulation, cell cycle, Foxo signaling, and Wnt signaling pathway are enriched among the up-regulated genes, while those involved in ion transport, cell adhesion, and oxidation-reduction are enriched among the down-regulated genes. Among the top up-regulated genes is FK506 binding protein 5 (Fkbp5), a member of the conserved immunophilin family. CRISPR/Cas9-mediated Fkbp5 deletion abolished ionocyte reactivation and proliferation. Pharmacological inhibition of Fkbp5 had similar effects. Further analyses showed that genetic deletion and inhibition of Fkbp5 impaired Akt signaling. Forced expression of a constitutively active form of Akt rescued the defects caused by Fkbp5 inhibition. These results uncover a previously unrecognized role of Fbkp5 in regulating the quiescence-proliferation decision via Akt signaling. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.27.530299v1?rss=1 Authors: Prescott, R. A., Pankow, A. P., de Vries, M., Crosse, K., Patel, R. S., Alu, M., Loomis, C., Torres, V., Koralov, S. B., Ivanova, E. N., Dittmann, M., Rosenberg, B. R. Abstract: The airway epithelium is composed of diverse cell types with specialized functions that mediate homeostasis and protect against respiratory pathogens. Human airway epithelial cultures at air-liquid interface (HAE) are a physiologically relevant in vitro model of this heterogeneous tissue, enabling numerous studies of airway disease. HAE cultures are classically derived from primary epithelial cells, the relatively limited passage capacity of which can limit experimental methods and study designs. BCi-NS1.1, a previously described and widely used basal cell line engineered to express hTERT, exhibits extended passage lifespan while retaining capacity for differentiation to HAE. However, gene expression and innate immune function in HAE derived from BCi-NS1.1 versus primary cells have not been fully characterized. Here, combining single cell RNA-Seq (scRNA-Seq), immunohistochemistry, and functional experimentation, we confirm at high resolution that BCi-NS1.1 and primary HAE cultures are largely similar in morphology, cell type composition, and overall transcriptional patterns. While we observed cell-type specific expression differences of several interferon stimulated genes in BCi-NS1.1 HAE cultures, we did not observe significant differences in susceptibility to infection with influenza A virus and Staphylococcus aureus. Taken together, our results further support BCi-NS1.1-derived HAE cultures as a valuable tool for the study of airway infectious disease. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.09.527850v1?rss=1 Authors: Fadjukov, J., Wienbar, S., Milicevic, N., Hakanen, S., Vihinen-Ranta, M., Ihalainen, T. O., Schwartz, G. W., Nymark, S. Abstract: Retinal pigment epithelium (RPE) at the back of the eye is a monolayer of cells with an extensive network of gap junctions that contributes to retinal health in a multitude of ways. One of those roles is the phagocytosis of photoreceptor outer segments. This renewal is under circadian regulation and peaks after light onset. Connexin 43 (Cx43) is the most predominantly expressed gap junction protein in RPE. In this study, we examine how gap junctions and specifically, Cx43 phosphorylation, contribute to phagocytosis in both human embryonic stem cell derived RPE and mouse RPE monolayers. We show that both Rac1 and CDK5 have differences in protein localization at different points in phagocytosis, and that by using their effectors, the capability of RPE for phagocytosis changes. CDK5 has not yet been reported in RPE tissue, and here we show that it likely regulates Cx43 localization and resulting electrical coupling. We find that gap junctions in RPE are temporally highly dynamic during phagocytosis and that regulation of gap junctions via phosphorylation is likely critical for maintaining eye health. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Hi Again and welcome back for episode 09 of our new season 3. Haven't you always wished to gain a greater understanding of the mysterious and complicated field of plastic procedures? Finally, now you can. Get connected and learn! Tune in and bookmark the “Dr. Jeffrey Roth's Looking Good Feeling Great Podcast” with his co-host, Darrell Craig Harris. For a start, you will be in no doubt about the love, passion, dedication, and empathy that Dr. Roth has for his patients and community. Plus, he always seems to add in a wonderful witty comment when you least expect it! (PS: for Dr. Jeffrey Roth's background, Bio, and reason for doing this show check out episode 01 of Season 1) Here's a taster for our new episode 09 - season 3. In this new episode 09, firstly a Big Shout Out to all of you around the world for continuing to listen in. That interest and support has helped our podcast achieve this recent milestone of 100K + downloads. PS: Now hitting @ 165+K :) Minimizing post-surgical scarring is achieved by doing it the right-way. Dr Roth says “You want to cut on tension and sew back up on non-tension.” Especially when sewing, you take as much tension off the wound as possible. Often in layers to achieve a very good construct, with little or no tension on the outer layer, known as the Epithelium. In plastic surgery this is a key factor to lay the groundwork for a healthy recovery, and provided the patient also fully participates in the healing process...then you are getting the results of your investment in looking good, and feeling great! BTW - Dr Roth has a new updated website - so check it out - the website link is below. Don't forget to contact Dr Roth and his team if you have any questions that you'd like discussed on upcoming podcast episodes. This is just for starters, listen in and hear a lot more fascinating information, we hope you enjoy this fun/fact-filled episode. So...remember that Dr. Roth is always keeping up to date with the latest procedures that are developed so that he and his care team can offer you the best they have on offer. PS: Don't forget if you have related questions or would like to hear about related plastic procedure topics. Please CONTACT our co-host Darrell Craig Harris, and he will endeavor to ask your plastic procedure-related question to Dr. Roth on air. You'll find all our contact email on the main page or through our social media channels - Look forward to hearing from you. Wow, and there's a lot more to hear... As this episode and future episodes progress you'll find YOU become more aware and gain a deeper appreciation of the complex world of plastic procedures - essentially a mix of the human body and mind engineering, coupled with great artistry and foresight. Plus, let's not forget ALL the special and helpful products and procedures. This is an industry that truly focuses on helping YOU Look Good and Feel Great... Download and listen in your vehicle or while on an airplane, on your lunch break, or just when you're taking time out for yourself. See You soon for Episode 10 of Season 3. PS: Check out Dr. Jeffrey Roth's Social media, we'd Love You to Like and follow, as it's a great way to keep up to date, or just download the Podcast to listen to offline on your iPhone or Android device. Check Us Out on our Social Media Channels :) https://twitter.com/drrothpodcast https://www.instagram.com/lookinggoodfeelinggreatpodcast/ https://www.facebook.com/lookinggoodpodcast/ https://www.jjrothmd.com/
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.08.25.505256v1?rss=1 Authors: Matsunaga, M., Yamamoto, R., Kita, T., Ohnishi, H., Yamamoto, N., Okano, T., Omori, K., Nakagawa, T. Abstract: In contrast to mammals, the avian cochlea, specifically the basilar papilla, can regenerate sensory hair cells, which involves fate conversion of supporting cells to hair cells. To determine the mechanisms for converting supporting cells to hair cells, we used single-cell RNA sequencing during hair cell regeneration in explant cultures of chick basilar papillae. We identified dynamic changes in the gene expression of supporting cells, and the pseudotime trajectory analysis demonstrated the stepwise fate conversion from supporting cells to hair cells. Initially, supporting cell identity was erased and transition to the precursor state occurred. A subsequent gain in hair cell identity progressed together with downregulation of precursor-state genes. Transforming growth factor beta receptor 1-mediated signaling was involved in induction of the initial step, and its inhibition resulted in suppression of hair cell regeneration. Our data provide new insights for understanding fate conversion from supporting cells to hair cells in avian basilar papillae. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer
Paper discussed in today's episode: The Type 2 Asthma Mediator IL-13 Inhibits Severe Acute Respiratory Syndrome Coronavirus 2 Infection of Bronchial Epithelium
PeerView Family Medicine & General Practice CME/CNE/CPE Video Podcast
Go online to PeerView.com/MRW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert in asthma discusses the role of the airway epithelium in severe asthma treatment. Upon completion of this activity, participants should be better able to: Apply the latest pathophysiologic insights into the role of epithelial alarmins in the development of inflammation and structural changes in the airways to the treatment of patients with severe asthma, Discuss the clinical implications of biologic treatment that is not limited by phenotype or biomarker for patients with severe asthma whose disease remains uncontrolled despite standard treatment, Identify patients with severe asthma who may be eligible for treatment with novel biologic therapies that target epithelial alarmins.
Go online to PeerView.com/MRW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert in asthma discusses the role of the airway epithelium in severe asthma treatment. Upon completion of this activity, participants should be better able to: Apply the latest pathophysiologic insights into the role of epithelial alarmins in the development of inflammation and structural changes in the airways to the treatment of patients with severe asthma, Discuss the clinical implications of biologic treatment that is not limited by phenotype or biomarker for patients with severe asthma whose disease remains uncontrolled despite standard treatment, Identify patients with severe asthma who may be eligible for treatment with novel biologic therapies that target epithelial alarmins.
Go online to PeerView.com/MRW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert in asthma discusses the role of the airway epithelium in severe asthma treatment. Upon completion of this activity, participants should be better able to: Apply the latest pathophysiologic insights into the role of epithelial alarmins in the development of inflammation and structural changes in the airways to the treatment of patients with severe asthma, Discuss the clinical implications of biologic treatment that is not limited by phenotype or biomarker for patients with severe asthma whose disease remains uncontrolled despite standard treatment, Identify patients with severe asthma who may be eligible for treatment with novel biologic therapies that target epithelial alarmins.
Go online to PeerView.com/MRW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert in asthma discusses the role of the airway epithelium in severe asthma treatment. Upon completion of this activity, participants should be better able to: Apply the latest pathophysiologic insights into the role of epithelial alarmins in the development of inflammation and structural changes in the airways to the treatment of patients with severe asthma, Discuss the clinical implications of biologic treatment that is not limited by phenotype or biomarker for patients with severe asthma whose disease remains uncontrolled despite standard treatment, Identify patients with severe asthma who may be eligible for treatment with novel biologic therapies that target epithelial alarmins.
PeerView Family Medicine & General Practice CME/CNE/CPE Audio Podcast
Go online to PeerView.com/MRW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert in asthma discusses the role of the airway epithelium in severe asthma treatment. Upon completion of this activity, participants should be better able to: Apply the latest pathophysiologic insights into the role of epithelial alarmins in the development of inflammation and structural changes in the airways to the treatment of patients with severe asthma, Discuss the clinical implications of biologic treatment that is not limited by phenotype or biomarker for patients with severe asthma whose disease remains uncontrolled despite standard treatment, Identify patients with severe asthma who may be eligible for treatment with novel biologic therapies that target epithelial alarmins.
Go online to PeerView.com/MRW860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this activity, an expert in asthma discusses the role of the airway epithelium in severe asthma treatment. Upon completion of this activity, participants should be better able to: Apply the latest pathophysiologic insights into the role of epithelial alarmins in the development of inflammation and structural changes in the airways to the treatment of patients with severe asthma, Discuss the clinical implications of biologic treatment that is not limited by phenotype or biomarker for patients with severe asthma whose disease remains uncontrolled despite standard treatment, Identify patients with severe asthma who may be eligible for treatment with novel biologic therapies that target epithelial alarmins.
Dr. Ophir Klein is the inaugural Executive Director of Cedars-Sinai Guerin Children's and the David and Meredith Kaplan Distinguished Chair in Children's Health. He discusses his work on intestinal epithelium regeneration, which he will present at the “Tissue Fibrosis and Repair: Mechanism, Human Disease, and Therapies” Keystone Symposium taking place from June 12-16th in Keystone, Colorado. He also talks about mechanisms of tooth development, analyzing three-dimensional facial images to diagnose genetic syndromes, and how parasitic infections affect the intestinal stem cell niche.
ATS 2022 starts May 13. Register today: conference.thoracic.orgPodcast CreditsWriter: Ryan Thomas, MDProducer: Ryan Thomas, MDReviewers: Christina Barreda, MDElizabeth Fiorino, MDReferences: Andreeva AV Regulation of surfactant secretion in alveolar type II cells 2007 AmJPhyLung Banfi C, Agostoni P. Surfactant protein B: From biochemistry to its potential role as diagnostic and prognostic marker in heart failure. Int J Cardiol. 2016 Oct 15;221:456-62 Chroneos ZC, et al. Pulmonary surfactant: an immunological perspective. Cell Physiology and Biochemistry 2010; 25: 13-26. Cole FS, Nogee LM, Hamvas A. Defects in surfactant synthesis: clinical implications. Pediatr Clin N Am 2006; 53: 911-927. Guillot-Alveolar epithelial cells Master regulators of lung homeostasis 2013 IntJBiochemCellBio Frerking I, et al. Pulmonary surfactant: functions, abnormalities, and therapeutic options. Intensive Care Med 2001; 27: 1699-1717. Herzog EL Knowns and Unknowns of the Alveolus PROCATS57778 Mason RJ. Biology of alveolar type II cells-2006-Respirology Murray and Nadel's Textbook of Respiratory Medicine 5th ed. Accessed via MDConsult. Nathan N Surfactant protein A: A key player in lung homeostasis IntJBioCellBio 2016 Nkadi PO, et al. An overview of pulmonary surfactant in the neonate: genetics, metabolism, and the role of surfactant in health and disease. Mol Genet Metab 2009; 97: 95-101. Whitsett JA, Wert SE, Weaver TE. Alveolar surfactant homeostasis and the pathogenesis of pulmonary disease. Annual Review of Medicine 2010; 61: 105-119. Wert SE, Whitsett JA, Nogee LM. Genetic disorders of surfactant dysfunction. Pediatr Dev Pathol. 2009; 12(4): 253-274.
What are the obstacles that stand between us and engineering functional lungs? Laura Niklason, MD, PhD outline the promises and challenges of lung regeneration. She details current studies that may unveil a roadmap for building functional lung aveolus. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 37580]
What are the obstacles that stand between us and engineering functional lungs? Laura Niklason, MD, PhD outline the promises and challenges of lung regeneration. She details current studies that may unveil a roadmap for building functional lung aveolus. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 37580]
What are the obstacles that stand between us and engineering functional lungs? Laura Niklason, MD, PhD outline the promises and challenges of lung regeneration. She details current studies that may unveil a roadmap for building functional lung aveolus. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 37580]
What are the obstacles that stand between us and engineering functional lungs? Laura Niklason, MD, PhD outline the promises and challenges of lung regeneration. She details current studies that may unveil a roadmap for building functional lung aveolus. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 37580]
What are the obstacles that stand between us and engineering functional lungs? Laura Niklason, MD, PhD outline the promises and challenges of lung regeneration. She details current studies that may unveil a roadmap for building functional lung aveolus. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 37580]
What are the obstacles that stand between us and engineering functional lungs? Laura Niklason, MD, PhD outline the promises and challenges of lung regeneration. She details current studies that may unveil a roadmap for building functional lung aveolus. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 37580]
What are the obstacles that stand between us and engineering functional lungs? Laura Niklason, MD, PhD outline the promises and challenges of lung regeneration. She details current studies that may unveil a roadmap for building functional lung aveolus. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 37580]
Aging-US published a Special Collection on Eye Disease which included "Loss of NAMPT in aging retinal pigment epithelium reduces NAD+ availability and promotes cellular senescence" which reported that retinal pigment epithelium performs numerous functions critical to retinal health and visual function. Here, the authors evaluated the temporal expression of key nicotinamide adenine dinucleotide -biosynthetic genes and associated levels of NAD+, a principal regulator of energy metabolism and cellular fate, in mouse RPE. They simulated in vitro the age-dependent decline in NAD+ and the related increase in RPE senescence in human and mouse primary RPE using the NAMPT inhibitor FK866 and demonstrated the positive impact of NAD+-enhancing therapies on RPE cell viability. This was confirmed in vivo in the RPE of mice injected sub-retinally with FK866 in the presence or absence of nicotinamide mononucleotide. Dr. Pamela M. Martin and Dr. Ravirajsinh N. Jadeja said, "The retinal pigment epithelium (RPE) performs numerous functions essential to normal retinal health and function." RPE serves as a physiologic barrier between the photoreceptor cells and the choroidal blood supply and in doing so, plays an essential role in protecting the retina from systemic insults by regulating immune responses and thereby limiting the entry of infectious or otherwise detrimental agents into retina. This is the premise of a number of recent studies including the present investigation in which we focused on nicotinamide adenine dinucleotide and factors governing its bioavailability in relation to the overall impact on RPE viability. NAD+, a central metabolic cofactor, plays a critical role in regulating cellular metabolism and energy homeostasis. The ratio of NAD+ to NADH regulates the activity of various enzymes essential to metabolic pathways including glycolysis, the Kreb's cycle, and fatty acid oxidation. There is a wealth of clinical and experimental data stemming from studies of other primary diseases of aging demonstrating clearly a generalized decline in the availability of NAD+ in association with increased age and the related reduction in the activity of a number of downstream metabolic pathways that contribute to the development and progression of degenerative processes. Members of the sirtuin family, poly ADP-ribose polymerases and the efficacy of therapies capable of impacting them have been evaluated in the context of aging retina and RPE. However, little attention has been given to upstream factors that regulate NAD+ biosynthesis, particularly in RPE. Given the importance of RPE to retinal health and function, in the present investigation we focused on evaluating the impact of NAD+ and factors that regulate its availability on RPE viability both in vivo and in vitro. This finding is highly relevant to the clinical management of AMD but perhaps also broadly to the management of other degenerative retinal diseases in which RPE is prominently affected. The Martin/Jadeja Research Team concluded in their Aging-US Research Output that these present data demonstrating an age-dependent decline in NAMPT expression and in turn, NAD+ generation in RPE which ultimately promotes RPE senescence supports strongly the rationale for enhancing NAMPT expression and associated NAD+ generation therapeutically. Based upon the present experimental observations, future preclinical studies evaluating NMN or other therapies that have a direct impact on NAMPT expression and NAD+ metabolism in the context of aging and age-related retinal disease development and progression are highly warranted. Full Text - https://www.aging-us.com/article/101469/text Correspondence to: Pamela M. Martin email: pmmartin@augusta.edu and Ravirajsinh N. Jadeja email: rjadeja@augusta.edu Keywords: retinal pigment epithelium (RPE), aging, age-related macular degeneration, NAD+, NAMPT, senescence, SIRT1
Aging-US published "A model of the aged lung epithelium in idiopathic pulmonary fibrosis" which reported that Iiopathic pulmonary fibrosis (IPF) is an age-related disorder that carries a universally poor prognosis. By exposing mouse alveolar epithelial cells to repeated, low doses of bleomycin, instead of usual one-time exposures, the authors uncovered changes strikingly similar to those in the IPF lung epithelium. They propose that this simple yet powerful tool could help uncover new biological mechanisms and assist in developing new pharmacological tools to treat the disease. Dr. Ross Summer from The Jane and Leonard Korman Respiratory Institute as well as Dr. Freddy Romero from The Baylor College of Medicine said, "Idiopathic pulmonary fibrosis (IPF) represents one of the most aggressive and irreversible lung diseases, has an unknown etiology, and limited therapeutic options." IPF arises from low-grade insults to the alveolar epithelium, which exhaust stem cell capacity and activate pathways that result in progressive tissue remodeling. Age represents the most significant risk factor for the development of IPF. Senescent cells are believed to drive immune cell and fibroblast activation via their production of secretory proteins (SASP), such as IL-6, TNF-β and TGF-β. Emerging evidence indicates that experimentally-induced pulmonary fibrosis can be ameliorated by targeting senescent cells for destruction [15]. This suggests a role for senolytic therapies in the treatment of IPf. The Summer/Romero Research Team concluded in their Aging-US Research Output, "we describe a novel model of the IPF lung epithelium that displays many characteristics of the dysfunctional IPF alveolar epithelium. Given its low cost and ease of implementation, we believe our model is ideally suited for uncovering the molecular underpinnings driving mitochondrial dysfunction, cellular senescence and loss of proteostasis in IPF. Further, we believe our model is also ideally suited for high throughput testing of novel pharmacological compounds directed at the alveolar epithelium. This includes drugs aimed at eliminating dysfunction epithelial cells, such as senolytic medications and agents that aim to restore health to the IPF alveolar epithelium" DOI - https://doi.org/10.18632/aging.203291 Full Text - https://www.aging-us.com/article/203291/text Correspondence to: Ross Summer email: Ross.Summer@Jefferson.edu and Freddy Romero email: Freddy.RomeroVasquez@bcm.edu Keywords: aging, IPF, mitochondria, proteostasis, epithelial cells About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways. To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM
Epithelium is one of the four basic tissue types (the other three are muscle tissue, nerve tissue, and connective tissue). It is found throughout the body—covering it; lining organs, vessels, and cavities; and forming glands. It absorbs nutrients, transports electrolytes, secretes hormones, and regulates body temperature by producing sweat. We begin with some general principles of how epithelial tissue is organized, and then we describe its various components. After listening to this AudioBrick, you should be able to: List the two types of epithelium (covering/lining and glandular) and describe their functions. Describe the structure and histologic features of epithelial tissue. Explain how covering/lining epithelium is classified. Describe the histologic features of glandular epithelium. Describe the five types of epithelial intercellular junctions. You can also check out the original brick on the Histology of Epithelial Tissue from our Musculoskeletal, Skin, and Connective Tissue collection, which is available for free. Learn more about Rx Bricks by signing up for a free USMLE-Rx account: www.usmle-rx.com You will get 5 days of full access to our Rx360+ program, including nearly 800 Rx Bricks. After the 5-day period, you will still be able to access over 150 free bricks, including the entire collections for General Microbiology and Cellular and Molecular Biology. *** If you enjoyed this episode, we'd love for you to leave a review on Apple Podcasts. It helps with our visibility, and the more med students (or future med students) listen to the podcast, the more we can provide to the future physicians of the world. Follow USMLE-Rx at: Facebook: www.facebook.com/usmlerx Blog: www.firstaidteam.com Twitter: https://twitter.com/firstaidteam Instagram: https://www.instagram.com/firstaidteam/ YouTube: www.youtube.com/USMLERX Learn how you can access over 150 of our bricks for FREE: https://usmlerx.wpengine.com/free-bricks/
What is a tissue. Types of epithelium. Classification of epithelial tissue. Classification of exocrine glands. Modifications of cell surface epithelium --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app --- Send in a voice message: https://anchor.fm/oge-osondu/message
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.27.222976v1?rss=1 Authors: Everetts, N., Worley, M. I., Yasutomi, R., Yosef, N., Hariharan, I. K. Abstract: In both vertebrates and invertebrates, generating a functional appendage requires interactions between ectoderm-derived epithelia and mesoderm-derived cells. To investigate such interactions, we used single-cell transcriptomics to generate a cell atlas of the Drosophila wing disc at two time points during development. Using these data, we investigate gene expression using a multi-layered model of the wing disc and catalogued ligand-receptor pairs that could mediate signaling between epithelial cells and adult muscle precursors (AMPs). We found that localized expression of the FGF ligands, Thisbe and Pyramus, in the disc epithelium regulates the number and location of the AMPs. In addition, Hedgehog ligand from the epithelium activates a specific transcriptional program within adjacent AMP cells, which is critical for proper formation of a subset of the direct flight muscles. More generally, our annotated atlas provides a global view of potential cell-cell interactions between subpopulations of epithelial and myogenic cells. Copy rights belong to original authors. Visit the link for more info
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.15.201723v1?rss=1 Authors: La Cunza, N., Tan, L. X., Rathnasamy, G., Thamban, T., Germer, C. J., Toops, K. A., Lakkaraju, A. Abstract: The retinal pigment epithelium (RPE) is the site of initial damage leading to photoreceptor degeneration and vision loss in age-related macular degeneration (AMD). Genetic and histopathological studies implicate cholesterol dysregulation in AMD; yet mechanisms linking cholesterol to RPE injury and drusen formation remain poorly understood. Especially enigmatic are allelic variants of the cholesterol transporter APOE, major risk modifiers in Alzheimer's disease that show reversed risk associations with AMD. Here, we investigated how ApoE isoforms modulate RPE health using live-cell imaging of primary RPE cultures and high-resolution imaging of human donor tissue. We show that the AMD-protective ApoE4 efficiently transports cholesterol and safeguards RPE homeostasis despite cellular stress. In contrast, ApoE2-expressing RPE accumulate cholesterol, which promotes autophagic deficits and complement-mediated mitochondrial fragmentation. Redox-related order-disorder phase transitions in ApoE2 drive the formation of intracellular biomolecular condensates as potential drusen precursors. Drugs that restore mitochondrial function limit condensate formation in ApoE2-RPE. Autophagic and mitochondrial defects correlate with intracellular ApoE aggregates in AMD donor RPE. Our study elucidates how AMD risk variants act as tipping points to divert the RPE from normal aging towards AMD by disrupting critical metabolic functions, and identifies mitochondrial stress-mediated aberrant phase transitions as a novel mechanism of drusen biogenesis. Copy rights belong to original authors. Visit the link for more info
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.16.151704v1?rss=1 Authors: Bryche, B., Saint-Albin Deliot, A., Murri, S., Lacote, S., Pulido, C., Ar Gouilh, M., Lesellier, S., Servat, A., Wasniewski, M., Picard-Meyer, E., Montchartre-Leroy, E., Volmer, R., Rampin, O., Le Goffic, R., Marianneau, P., Meunier, N. Abstract: Anosmia is one of the most prevalent symptoms of SARS-CoV-2 infection during the COVID-19 pandemic. However, the cellular mechanism behind the sudden loss of smell has not yet been investigated. The initial step of odour detection takes place in the pseudostratified olfactory epithelium (OE) mainly composed of olfactory sensory neurons surrounded by supporting cells known as sustentacular cells. The olfactory neurons project their axons to the olfactory bulb in the central nervous system offering a potential pathway for pathogens to enter the central nervous system by bypassing the blood brain barrier. In the present study, we explored the impact of SARS-COV-2 infection on the olfactory system in golden Syrian hamsters. We observed massive damage of the OE as early as 2 days post nasal instillation of SARS-CoV-2, resulting in a major loss of cilia necessary for odour detection. These damages were associated with infection of a large proportion of sustentacular cells but not of olfactory neurons, and we did not detect any presence of the virus in the olfactory bulbs. We observed massive infiltration of immune cells in the OE and lamina propria of infected animals, which may contribute to the desquamation of the OE. The OE was partially restored 14 days post infection. Anosmia observed in COVID-19 patient is therefore likely to be linked to a massive and fast desquamation of the OE following sustentacular cells infection with SARS-CoV-2 and subsequent recruitment of immune cells in the OE and lamina propria. Copy rights belong to original authors. Visit the link for more info
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.05.21.107110v1?rss=1 Authors: Najjar, S. A., Ejoh, L. L., Loeza-Alcocer, E., Edwards, B. S., Smith-Edwards, K. M., Epouhe, A. Y., Gold, M. S., Davis, B. M., Albers, K. M. Abstract: Visceral pain is a prevalent symptom of inflammatory bowel disease (IBD) that can be difficult to treat. This pain and hypersensitivity are mediated by extrinsic primary afferent neurons (ExPANs) that innervate the colon. Recent studies indicate that the colon epithelium contributes to initiating ExPAN firing and nociceptive responses. Based on these findings we hypothesized that the epithelium contributes to inflammation-induced hypersensitivity. A key prediction of this hypothesis is that inhibition of the epithelium would attenuate nociceptive signaling and inflammatory hypersensitivity. To test this hypothesis, the inhibitory yellow light activated protein archaerhodopsin was targeted to the intestinal epithelium (villin-Arch) or the ExPANs (TRPV1-Arch) that innervate the colon. Visceral sensitivity was assessed by measuring the visceromotor response (VMR) to colorectal distension (CRD), with and without yellow light illumination of the colon lumen. Inhibition of the colon epithelium in healthy villin-Arch mice significantly diminished the CRD-induced VMR. Direct inhibition of ExPANs during CRD using TRPV1-Arch mice showed that ExPAN and epithelial inhibition were similarly effective in reducing the VMR to CRD. We then investigated the effect of epithelial and ExPAN inhibition in the dextran sulfate sodium (DSS) model of inflammatory bowel disease (IBD). Inhibition of the colon epithelium significantly decreased DSS-induced hypersensitivity and was comparable to inhibition of ExPANS. Together these results reveal the potential of targeting the colon epithelium for treatment of pain. Copy rights belong to original authors. Visit the link for more info
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.05.14.096016v1?rss=1 Authors: Baxter, B. D., Larson, E. D., Feinstein, P., Polese, A. G., Bubak, A. N., Niemeyer, C. S., Merle, L., Shepherd, D., Ramakrishnan, V. R., Nagel, M. A., Restrepo, D. Abstract: Understanding viral infection of the olfactory epithelium is essential because smell loss can occur with coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), and because the olfactory nerve is an important route of entry for viruses to the central nervous system. Specialized chemosensory epithelial cells that express the transient receptor potential cation channel subfamily M member 5 (TRPM5) are found throughout the airways and intestinal epithelium and are involved in responses to viral infection. Herein we performed deep transcriptional profiling of olfactory epithelial cells sorted by flow cytometry based on the expression of fluorescent protein markers for olfactory sensory neurons and TRPM5. We find profuse expression of transcripts involved in inflammation, immunity and viral infection in TRPM5-expressing microvillous cells and olfactory sensory neurons. These cells express the Tmprss2 transcript that encodes for a serine protease that primes the SARS-CoV-2 spike protein before entry into host cells. Our study provides new insights into a potential role for TRPM5-expressing cells in viral infection of the olfactory epithelium. Copy rights belong to original authors. Visit the link for more info
Professor Susan Anderson shows us what the layers of cells that cover our outsides and our insides look like down the microscope. Learn how to recognise each type of epithelium and why they need to be different. Also learn the suprising meaning of the word epithelium...
(Histology) --- Support this podcast: https://anchor.fm/brad-richardson/support
(Histology) --- Support this podcast: https://anchor.fm/brad-richardson/support
Hosts: Vincent Racaniello, Dickson Despommier, and Daniel Griffin The TWiPtastic trio solves the case of the Surfer from Switzerland, and reveal how taste-chemosensory tuft cells in the gut regulate immune responses to parasites. Links for this episode: Taste-chemosensory cells and parasite gut immunity (Science) Image credit Letters read on TWiP 107 This episode is sponsored by ASM Agar Art Contest and ASM Microbe 2016 Case study for TWiP 107 Todays case is a fun case about a 45 year old gentleman from Assam India, with sixteen years of fever, abdominal pain, darkening of skin, yellowing of eyes. Farmer, does not have much energy. Works barefoot in fields. Fever occurs every other day. Prior medical problems, nothing out of the ordinary. No surgeries, no meds, has never seen physician. Married, kids, no extramarital affairs, HIV negative, eats mostly cooked vegetables. Lives in concrete house, no screens, mosquito netting. Other people in area have similar problems. Water comes from pump, fill plastic jugs. Been in Assam sick his whole life, finally came to regional med center for evaluation. Underweight. No pets. Dogs around, avoids dogs. Cows, monkeys are around. Fair appetite. Exam: febrile, in face can see darkening which is increasing, also extremities. Whites of eyes are yellow (jaundiced). Striking is has a very large liver, spleen. Elevated bilirubin. Some increased liver enzymes. No physical scarring or lesions. Send your diagnosis to twip@microbe.tv Send your questions and comments to twip@microbe.tv
Research from Erik Danen and colleagues suggests that, although therapies that interfere with cell adhesion signaling may slow the growth of some types of breast cancer, they may promote metastasis.
Steve Rogers and Mark Peifer identify the G protein–coupled receptor Mist as the receptor for Fog, a secreted factor that drives gastrulation in fruit fly embryos.
Peter Parker, Mark Linch, and Neil McDonald discuss a motif in an atypical protein kinase that mediates interactions with cell polarity substrates and is mutated in some cancers.
File download (84:39 mins | 19 MB)
Although many aspects of ovarian differentiation have been established,comparatively little is known about prenatal follicle formation anddifferentiation of bovine ovaries. The objective of this investigationwas to study the role of the surface epithelium during the developmentof germ cell nests, germ cell cords and follicle formation in the fetalbovine ovary. Associated important proliferation and apoptotic featureswere further investigated. Additionally, the expression pattern of theS100 protein was detected. A strong increase of mitotic figures wasdetected in the surface epithelium, germ cell nests and germ cell cordsof ovaries with a crown-rump length (CRL) of 13.0-58.0 cm. Oocytes werepositively stained with S100 in bovine ovaries from fetuses with a CRLof 21.0 cm. The staining intensity enhanced parallel to increasingoocyte and follicle sizes during the ovary development. In later stages,a strong staining for S100 was observed in healthy oocytes incontradistinction to atretic oocytes where no expression of the S100protein could be found. In conclusion, increasing mitosis index ofsurface epithelium cells, as well as oogonia directly beneath thesurface epithelium, in combination with open surface connection duringstages from a CRL of 11.0-94.0 cm of bovine fetal ovaries could play animportant role in the period of time of ongoing folliculogenesis andderivation of granulosa cells. Additionally, S100-positive oocytes inprimordial and later follicle stages joined by a high rate ofKi67-positive index in surrounding granulosa cells indicate that in theoocytes the S100 protein can perhaps be a useful marker for intactoocytes in bovine ovaries.
ZOOL 1090: Introduction to Human Anatomy and Physiology - DE
Episode 05: Histology: Introduction, Muscle Tissue, Epithelium. Full video episode of Introduction to Human Anatomy and Physiology, a university course produced by Distance Education at Utah Valley University in the USA.
John Doorbar, Division of Virology, National Institute for Medical Research, London, UK speaks on "Papillomavirus Life Cycle Regulation in Infected Epithelium". This seminar has been recorded by ICGEB Trieste
Background Cumulative light exposure is significantly associated with progression of age-related macular degeneration (AMD). Inhibition of vascular endothelial growth factor is the main target of current antiangiogenic treatment strategies in AMD. However, other growth factors, such as platelet-derived growth factor (PDGF) and placenta growth factor (PlGF), have a substantial impact on development of AMD. Previous reports indicate that sorafenib, an oral multikinase inhibitor, might have beneficial effects on exudative AMD. This study investigates the effects of sorafenib on light-induced overexpression of growth factors in human retinal pigment epithelial (RPE) cells. Methods Primary human RPE cells were exposed to white light and incubated with sorafenib. Viability, expression, and secretion of VEGF-A, PDGF-BB, and PlGF and their mRNA were determined by reverse transcription-polymerase chain reactions, immunohistochemistry and enzyme-linked immunosorbent assays. Results Light exposure decreased cell viability and increased expression and secretion of VEGF-A, PDGF-BB and PlGF. These light-induced effects were significantly reduced when cells were treated with sorafenib at a dose of 1 mu g/ml. Conclusion The results show that sorafenib has promising properties as a potential antiangiogenic treatment for AMD.
Learn how bladder epithelium regenerates after infection (0:53) and which amino acids are involved in developing insulin resistance (9:50). Hear the latest news about regulatory T cells (14:37).
Fakultät für Chemie und Pharmazie - Digitale Hochschulschriften der LMU - Teil 03/06
Fri, 9 May 2008 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/12502/ https://edoc.ub.uni-muenchen.de/12502/1/Lorenz-Baath_Katrin.pdf Lorenz-Baath, Katrin ddc:540, ddc:500, F
Fakultät für Chemie und Pharmazie - Digitale Hochschulschriften der LMU - Teil 02/06
Inhalational anthrax is an acute infectious disease caused by exposure of the lungs to B. anthracis spores. Alveolar macrophages engulf spores causing them to germinate to the vegetative form of B. anthracis, which secretes edema toxin (ET)and lethal toxin (LT). The pathogenesis of inhalational anthrax is characterized by flu-like symptoms, respiratory distress, meningitis and shock, which is fatal in almost all cases. The mechanism behind the respiratory distress is not well understood. Therefore, our goal was to determine the effects of lethal toxin in the human lung epithelium. To study alterations in a more physiological setting, we developed a differentiated, polarized lung epithelial system. Lethal toxin exposure disrupted the lung barrier function and wound healing. Assembly defects of junction proteins and additional multicellular junction sites resulted in a higher permeability. Pretreatment with keratinocyte growth factor (KGF) and dexamethasone increased the viability, resulting in the rescue of the permeability changes. Upon LT treatment, a more rigid cytoskeleton was observed, evidenced by enhanced actin stress fiber formations and tubulin stabilization. Cytoskeleton and adhesion alterations prevented the epithelial cells from polarization, directed migration, and wound healing. The MAPK pathway and Cdc42 activity might be partially responsible for these motility defects. Lethal toxin is known to induce rapid cell death in murine macrophages. In contrast, human epithelial cells are more resistant to the cytotoxic effect of LT. By following the growth of epithelial cells after LT treatment, we observed inhibited cell proliferation due to a cell cycle arrest in the G1 phase. Surprisingly, biotinylated lethal factor did not induce cytotoxicity in murine macrophages. This is not due to an internalization or proteolytic activity defect; instead changes in the mitochondrial potential and proteasome activity were observed. Biotinylated LT did not reduce proteasome activity as seen in LT treated cells and caused hypopolarization of the mitochondria. However, it is possible that biotinylation of lethal toxin could prevent interaction of LT with proteins that induce cell death. The major challenge for anthrax treatment is to find a treatment, which can act faster, is easy to use and can bring patient out of the dangerous physiological state in late pathogenesis. Our study has implications in saving the viability and barrier function of lung epithelial cells. One can devise better dosage and delivery of KGF and dexamethasone as treatment modality for post anthrax exposure to reduce respiratory distress. Furthermore, overcoming the cell cycle arrest by the development of a drug would reduce the damage of lung epithelial cells and induce proliferation. The discovery that biotinylated LT is non-toxic to murine macrophages could revolutionize treatment of anthrax infection. Exploring the types of posttranslational modifications of LT that decrease toxicity and finding the mechanism behind it might, lead to therapies that directly counteract the effects of the lethal toxin in vivo.
Changes in ATP-induced increase in {[}Ca2+], during collecting duct ontogeny were studied in primary monolayer cultures of mouse ureteric bud (UB) and cortical collecting duct (CCD) cells by Fura-PE3 fluorescence ratio imaging. In UB (embryonic day E14 and postnatal day P1) the ATIP-stimulated increase (EC50 approximate to 1 muM) in fluorescence ratio (DeltaR(ATP)) was independent of extracellular Ca2+ and insensitive to the P2 purinoceptor-antagonist suramin (1 mM). From day P7 onward when CCD morphogenesis had been completed DeltaR(ATP) increased and became dependent on extracellular Ca2+. This ATP-stimulated Ca2+ entry into CCD cells was non-capacitative and suramin (11 mM)insensitive, but sensitive to nifedipine (30 muM) and enhanced by Bay K8644 (15 muM), a blocker and an agonist of L-type Ca2+ channels, respectively. Quantitative RT-PCR demonstrated similar mRNA expression of L-type Ca2+ channel alpha1-subunit, P2Y(1), P2Y(2), and P2X(4b) purinoceptors in UB and CCD monolayers while the abundance of P2X(4) mRNA increased with CCD morphogenesis. In conclusion, both embryonic and postnatal cells express probably P2Y(2)-stimulated Ca2+ release from intracellular stores. With development, the CCD epithelium acquires ATP-stimulated Ca2+ entry via L-type Ca2+ channels. This pathway might by mediated by the increasing expression of P2X(4)-receptors resulting in an increasing ATP-dependent membrane depolarization and activation of L-type Ca2+ channels. Copyright (C) 2002 S. Karger AG, Basel.
Background: 5-Aminolevulinic acid (5-ALA)-induced protoporphyrin IX (PPIX) fluorescence improves the differentiation of tumor and normal tissue in the bladder, skin and brain. Objective: The kinetics of 5-ALA-induced protoporphyrin IX (PPIX) fluorescence in organ cultures of normal human bronchial epithelium and cocultures of bronchial epithelium and tumor have been studied. Methods: Cultured biopsies of bronchial epithelium were exposed for 5 or 15 min, or continuously to 5-ALA. PPIX fluorescence was quantified for up to 300 min by spectroscopy. Cocultures of normal bronchial epithelium and a non-small-cell lung cancer cell line (EPLC-32M1) were incubated with 5-ALA. Space-resolved fluorescence microscopy was used to quantify PPIX fluorescence kinetics in the tumor and normal epithelium. Results: In cultures of normal epithelium, PPIX fluorescence kinetics were shown to depend on the duration of exposure to 5-ALA. There was a trend to higher fluorescence intensities with longer exposure times. In cocultures of bronchial epithelium and tumor, increases of fluorescence intensity were significantly greater in the tumor. Best tumor/normal tissue fluorescence ratios were found between 110 and 160 min after exposure to 5-ALA. Conclusion: Data obtained in this coculture system of bronchial epithelium and tumor is valuable to optimize modalities of fluorescence bronchoscopy for the diagnosis of early bronchial carcinoma. Copyright (C) 2002 S. Karger AG, Basel.
associated with aging. Thus, the question arises whether or not a correlation exists between the well known prostatic androgen and estrogen accumulation and aging. To address this question, we measured 5a-dihydrotestosterone (DHT), testosterone, estradiol, and estrone in epithelium and stroma of six normal (NPR) and 19 BPH and correlated the values with the age of the donors (26-87 yr). The mean DHT level in NPR epithelium was significantly higher than in NPR stroma, and also significantly higher than in epithelium and stroma of BPH. The epithelial DHT level of NPR and BPH decreased with age, the correlation being statistically significant. The stromal DHT level of NPR and BPH showed no correlation with age. Concerning testosterone, generally rather low values were found which showed no correlation with age. The mean levels of estradiol and estrone were significantly higher in BPH stroma as compared to BPH epithelium as well as to NPR epithelium and stroma. In NPR, the mean levels of estradiol and estrone were significantly higher in epithelium than stroma. In NPR and BPH, the stromal estradiol and estrone levels increased significantly with age. In epithelium such a correlation between the estrogen levels and age was not found. Our results indicate that the prostatic accumulation of DHT, estradiol, and estrone is in part intimately correlated with aging, leading with increasing age to a dramatic increase of the estrogen/androgen ratio particularly in stroma of BPH.
Fri, 1 Jan 1993 12:00:00 +0100 http://epub.ub.uni-muenchen.de/4047/ http://epub.ub.uni-muenchen.de/4047/1/026.pdf Gao, L.; Wagner, Ernst; Cotten, Matt; Agarwal, Santosh; Harris, C. E.; Romer, M.; Miller, L.; Hu, P.-C.; Curiel, David T. Gao, L.; Wagner, Ernst; Cotten, Matt; Agarwal, Santosh; Harris, C. E.; Romer, M.; Miller, L.; Hu, P.-C. und Curiel, David T. (1993): Direct in vivo gene transfer to the airway epithelium employing adenovirus-polylysine-DNA complexes. In: Human Gene Therapy, Vol. 4: pp. 17-24.